1. Field of the Invention
This invention relates to urogenital and gastrointestinal surgery.
2. Description of the Related Art
Female genital prolapse has long plagued women. It is estimated by the U.S. National Center for Health Statistics that 247,000 operations for genital prolapse were performed in 1998. With the increasing age of the U.S. population, these problems will likely assume additional importance.
The common clinical symptoms of vaginal prolapse are largely related to the fact that the vagina is inappropriately serving the role of a structural layer between intra-abdominal pressure and atmospheric pressure. This pressure differential puts tension on the supporting structures of the vagina, causing a “dragging feeling” where the tissues connect to the pelvic wall or a sacral backache due to traction on the uterosacral ligaments. Exposure of the moist vaginal walls leads to a feeling of perineal wetness and can lead to ulceration of the exposed vaginal wall. Vaginal prolapse may also result in loss of urethral support due to displacement of the normal structural relationship, resulting in stress urinary incontinence. Certain disruptions of the normal structural relationships can result in urinary retention, as well. Stretching of the bladder base is associated with vaginal prolapse and can result in complaints of increased urinary urgency and frequency. Other symptoms, such as anal incontinence and related bowel symptoms, and sexual dysfunction are also frequently seen with vaginal prolapse.
Anterior vaginal wall prolapse causes the vaginal wall to fail to hold the bladder in place. This condition, in which the bladder sags or drops into the vagina, is termed a cystocele. There are two types of cystocele caused by anterior vaginal wall prolapse. Paravaginal defect is caused by weakness in the lateral supports (pubourethral ligaments and attachment of the bladder to the endopelvic fascia); central defect is caused by weakness in the central supports. There may also be a transverse defect, causing cystocele across the vagina.
Posterior vaginal wall prolapse results in descent of the rectum into the vagina, often termed a rectocele, or the presence of small intestine in a hernia sac between the rectum and vagina, called an enterocele. Broadly, there are four types based on suspected etiology. Congenital enteroceles are thought to occur because of failure of fusion or reopening of the fused peritoneal leaves down to the perineal body. Posthysterectomy vault prolapses may be “pulsion” types that are caused by pushing with increased intra-abdominal pressure. They may occur because of failure to reapproximate the superior aspects of the pubocervical fascia and the rectovaginal fascia at the time of surgery. Enteroceles that are associated with cystocele and rectocele may be from “traction” or pulling down of the vaginal vault by the prolapsing organs. Finally, iatrogenic prolapses may occur after a surgical procedure that changes the vaginal axis, such as certain surgical procedures for treatment of incontinence. With regard to rectoceles, low rectoceles may result from disruption of connective tissue supports in the distal posterior vaginal wall, perineal membrane, and perineal body. Mid-vaginal and high rectoceles may result from loss of lateral supports or defects in the rectovaginal septum. High rectoceles may result from loss of apical vaginal supports. Posterior or posthysterectomy enteroceles may accompany rectoceles.
Several factors have been implicated as being involved in genital prolapse in women. It is thought that individual women have differing inherent strength of the relevant connective tissue. Further, loss of connective tissue strength might be associated with damage at childbirth, deterioration with age, poor collagen repair mechanisms, and poor nutrition. Loss of muscle strength might be associated with neuromuscular damage during childbirth, neural damage from chronic straining, and metabolic diseases that affect muscle function. Other factors involved in prolapse include increased loads on the supportive system, as seen in prolonged lifting or chronic coughing from chronic pulmonary disease, or some disturbance in the balance of the structural support of the genital organs. Obesity, constipation, and a history of hysterectomy have also been implicated as possible factors.
As noted, vaginal prolapse and the concomitant anterior cystocele can lead to discomfort, urinary incontinence, and incomplete emptying of the bladder. Posterior vaginal prolapse may additionally cause defecatory problems, such as tenesmus, constipation, and anal incontinence. Furthermore, apart from the physical symptoms, vaginal prolapse has been shown to result in a lower quality of life for its sufferers, including feeling less attractive, less feminine, and less sexually attractive.
Vaginal prolapse develops when intra-abdominal pressure pushes the vagina outside the body. In a normal situation, the levator ani muscles close the pelvic floor. This results in little force being applied to the fascia and ligaments that support the genital organs. Increases in abdominal pressure, failure of the muscles to keep the pelvic floor closed, and damage to the ligaments and fascia all contribute to the development of prolapse. In addition, if a woman has a hysterectomy, the vaginal angle may be altered, causing increased pressure at a more acute angle, accelerating the prolapse.
There are generally two different types of tissue that make up the supportive structure of the vagina and uterus. First, there are fibrous connective tissues that attach these organs to the pelvic walls (cardinal and uterosacral ligaments; pubocervical and rectovaginal fascia). Second, the levator ani muscles close the pelvic floor so the organs can rest on the muscular shelf thereby provided. It is when damage to the muscles opens the pelvic floor or during the trauma of childbirth that the fascia and ligaments are strained. Breaks in the fascia allow the wall of the vagina or cervix to prolapse downward.
Put another way, support for the pelvic structures can be described in three levels. Level 1 is the suspension of the apex of the vagina from the sides of the sacrum. The principle anatomical structure is the cardinal uterosacral ligament complex, which suspends the vagina while allowing some vertical mobility. Normally, the cervix of a woman will not descend below the plane of the ischial spines. Damage to Level 1 supports permit the uterus and upper vagina to telescope downward. Symptoms of Level 1 failure include pelvic heaviness, pressure, and urinary incontinence. A cervix-first prolapse, where the cervix inverts, is seen in complete Level 1 failure.
Level 2 concerns the lateral attachment of the vagina to the pelvic side wall. This level prevents prolapse of the bladder and the rectum into the vagina, i.e. cystocele or rectocele. The pubocervical and rectovaginal fascia provide this mid-vaginal suspensory mechanism. Level 2 support failure results in eversion of the vaginal walls, as opposed to inversion as seen in Level 1 failures. Symptoms of Level 2 failure include symptoms related to visceral failure, such as stress incontinence, voiding difficulty, fecal incontinence, or incomplete rectal evacuation. Sexual symptoms, such as painful intercourse and decreased libido are also seen.
Level 3 is near the opening of the vagina where the muscles of the levator sling and the distal portion of the vagina are joined to the perineal body. These distal vaginal defects can result from or exacerbate levator muscle flaccidity, which, if present with Level 2 failures, can result in worsening of any posterior or anterior eversion of the vagina. Level 3 failures can result in urinary and anal incontinence, and can result in vaginal dryness, chronic vaginitis, and loss of vaginal tightness due to the concomitant gaping of the lower vagina.
Level 3 support includes the perineum. The perineum is the entirety of the pelvic outlet inferior to the pelvic floor. The area between the vagina and anus is called the perineal body. The borders of the female perineum are the ischiopubic rami, ischial tuberosities, sacrotuberous ligaments and coccyx. A line connecting the ischial tuberosities divides the perineum into the urogenital triangle anteriorly and the anal triangle posteriorly. In the standing position the perineal body is oriented horizontally. The urogenital triangle is oriented horizontally and tilted upward so that it faces more anteriorly while the anal triangle is tilted upward so that it faces more posteriorly.
The perineal membrane is a thick fibrous sheet that spans the urogenital triangle. It attaches laterally to the pubic arch and has a free posterior margin anchored in the midline by the perineal body. The urethra and vagina penetrate through a hiatus in the perineal membrane (the urogenital hiatus) to exit at the vestibule. The perineal membrane, therefore, provides fixation of the distal urethra, distal vagina, and the perineal body to the pubic arches.
The urogenital triangle is divided into a superficial and deep perineal space by the perineal membrane. The superficial perineal space contains the superficial perineal muscles (ischiocavemosus, bulbospongiosus, superficial transverse perineal muscles), the erectile tissue of the clitoris, the vestibular bulbs, and Bartholin's glands. The deep perineal space lies deep to the perineal membrane and inferior to the levator ani muscles. Within this thin space lie the external urethral sphincter and the urethrovaginalis, compressor urethrae, and deep transverse perineal muscles. The urethrovaginalis and compressor urethrae muscles provide accessory sphincter function to the urethra. The urethrovaginalis muscle surrounds the distal urethra and vagina without passing between them and therefore acts as a sphincter to the vagina as well as to the distal urethra. The deep transverse perineal muscle, along with its superficial counterpart, serves to stabilize the position of the perineal body and inferior border of the perineal membrane.
The perineal body marks the point of convergence of the bulbospongiosus muscle, superficial and deep perinea, perineal membrane, external anal sphincter, posterior vaginal muscularis, and fibers from the puborectalis and pubococcygeus. The perineal body plays an important role in support of the distal vagina and in normal anorectal function.
The perineal body is supported centrally to the vagina. The connective tissue of the perineal body extends 2 to 4 cm cephalad from the hymenal ring along the posterior vaginal wall between the smooth muscle layers of the vagina and the rectum. This layer does not, however, extend the full length of the posterior vaginal wall. Therefore the perineal body gets more support for preventing downward movement from its lateral attachments. The perineal body is attached laterally to the ischial tuberosities. Superiorly, the support comes from the posterior lateral support of level 2. The posterior vaginal wall is attached laterally to the pelvic sidewall in a slightly more complex arrangement than the anterior vaginal wall. The distal half of the posterior vaginal wall fuses with the aponeurosis of the levator ani muscle from the perineal body along a line referred to as the arcus tendineus rectovaginalis. It converges with the arcus tendineus fasciae pelvis at a point 2 to 3 centimeters from the ischial spine and terminates at the ischial spine. Along the proximal ⅓ to ½ of the vagina, the anterior and posterior vaginal walls are both supported laterally to the arcus tendineus fasciae pelvis. Thus, in the proximal vagina, the lateral supports for the anterior and posterior vaginal wall are identical. This arrangement accounts for the H-shape of the distal vagina when viewed in cross-section and the flattened-tube configuration seen in the upper vagina. The Arcus tendineus rectovaginalis therefore gives direct support to the perineal body. Detachment of these lateral supports can lead to decent of the perineal body and prolapse of the posterior vaginal wall.
Level 3 support is also provided by the perineal membrane, the muscles of the deep perineal space, and the perineal body. These structures support and maintain the normal anatomical position of the urethra and the distal third of the vagina. At level 3, the vagina fuses with the urethra anteriorly and with the perineal body posteriorly. Disruption of the level 3 support anteriorly can result in urethral hypermobility and stress urinary incontinence. Disruption posteriorly may result in distal rectoceles and if there is detachment laterally from the ischial tuberosities with detachment of the lateral support from the arcus tendineus rectovaginalis there can also be perineal descent resulting in possible rectal prolapse and/or anal incontinence.
The vascular and nerve supply to the perineum, including the deep and superficial spaces, is provided by the pudendal neurovascular bundle. The pudental nerve innervates the striated urethral and anal sphincters in addition to the deep and superficial perineal muscles. Sensory innervation to the external genitalia also comes from the pudenal nerve. The pudendal nerve follows a complex course that originates from S2-S4 and travels behind the sacrospinous ligament just medial to the ischial spine, exiting the pelvis through the greater sciatic foramen. The nerve then enters the ischiorectal fossa through the lesser sciatic foramen and travels through the pudendal canal (Alcock's canal) on the medial aspect of the obturator internus muscles before separating into several terminal branches that terminate within the muscles and skin of the perineum. See Davila et al., Current Concepts in Pelvic Anatomy and Reconstructive Surgery, Cleveland Clinic Journal of Medicine. Supplement 4 to volume 72, December 2005, the entire contents of which are incorporated by reference.
When the perineal body becomes separated from it bilateral support attachments it will have downward movement of up to 3 to 6 cm. with increased abdominal pressure such as is generated with Valsalva for bowl movements. This movement causes the pudendal nerve to be repetitively stretched which can lead to denervation of the perineum structures. This nerve injury can be subtle and progressive. A common expression is the development of anal incontinence. When the perineal body is restabilized bilaterally the repetitive injury is prevented with the resolution of the incontinence. If the incontinence doesn't resolve then neural rehabilitative therapy may be required.
Treatment of vaginal prolapse and related conditions herein discussed is uncertain, and generally based on the symptoms of the prolapse. If symptoms are more severe, treatment is commonly by either surgery or pessary. Surgical options might include hysterectomy or by uterus-saving procedures. Such procedures may include abdominal or vaginal access routes. Sacralcolpopexy or sacrospinous fixation may be used. Anterior colporrhaphy is often utilized for treatment of anterior vaginal prolapse. In addition, methods of surgical repair using mesh or biological implants, or a combination thereof, to support the prolapsed organ in its appropriate position, have been developed, and may use either a transobturator or vaginal approach.
With regard to the rectocele, surgical treatment often includes the so-called posterior methods, better described as the anchorage of the involved tissues to the levator muscle (i.e., levator myorrhaphy). However, no matter the surgical approach, the rate of recurrence is unacceptably high, and the degree of satisfaction with the results of the surgeries is not acceptable.
The adaptation of synthetic mesh systems to support the repair of pelvic organ prolapse in women has, however, proven to result in improved results, reduced recurrences, and reduced morbidity associated with the repair. Examples of methods and apparatus useful for effecting repair of prolapse conditions include those disclosed in U.S. Publication 2005/0245787, herein expressly incorporated by reference, and in U.S. Publication 2005/0250977, also herein expressly incorporated by reference. U.S. Pat. No. 6,802,807, U.S. Pat. No. 6,911,003, U.S. Pat. No. 7,048,682, and U.S. Pat. No. 6,971,986 are also incorporated by reference.
Implants can be used to treat discrete prolapse conditions, or can be used to support the mid-urethra to relieve incontinence. However, if multiple levels of failure are present, multiple surgeries may be required. Indeed, some surgical options that show a good effect in treating certain symptoms, such as correcting the anatomical disorder and the concomitant sexual dysfunction, have a much less favorable effect in correcting obstructed defecation.
Consequently, there is a need for alternative methods and apparatus for repair of rectocele and other conditions associated with posterior pelvic floor pathology, particularly when several layers of support are desirable. Thus, the present invention is directed to providing such alternative methods and apparatus